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Organic acid transport
About: Organic acid transport is a research topic. Over the lifetime, 169 publications have been published within this topic receiving 293189 citations.
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TL;DR: It is hypothesized that the renal cortical uptake and proximal tubular toxicity of cephaloridine are related to a carrier-mediated transport system.
Abstract: Attempts to demonstrate net renal secretion of the antibiotic cephaloridine in mammals have been unsuccessful. Nevertheless, the acute proximal tubular necrosis produced by the drug can be prevented by prior administration of a variety of organic acid transport inhibitors. Studies were performed which confirmed the protective effect of probenecid against cephaloridine's nephrotoxicity its the rabbit. Renal uptake of cephaloridine was then studied in rabbits by giving single subcutaneous injections of the drug and measuring its concentration in serum, renal cortex and medulla 30 minutes later. Cortex/serum ratios (C/S) of cephaloridine were 12.2 ± S.E. 0.8 (10 animals) at doses of 100 mg/kg and 10.6 ± 0.6 (10) at doses of 25 mg/kg. These ratios were strikingly greater than those of inulin [C/S inulin = 1.5 ± 0.2 (5)]. Thus, cortical cephahoridine content was significantly greater than than can be accounted for by glomerular filtration alone. Prior administration of probenecid (100 mg/kg) to animals receiving 100 mg/kg of cephaloridine reduced C/S to 1.2 ± 0.1 (5). Administration of benzylpenicillin, given in increasing doses (100, 350 and 1000 mg/kg) to animals receiving 100 mg/kg of cephaloridine, resulted in decreases of C/S (7.0,2.9 and 1.1, respectively), suggesting a competitive inhibition of cortical cephaloridine uptake. Medulla/serum (M/S) cephaloridine concentrations were consistently lower than those of inulin [M/S inulin = 4.8 ± 0.6 (5)] and were significantly decreased by prior mannitol infusion, but they were unaffected by probenecid or benzylpenicillin. It is hypothesized that the renal cortical uptake and proximal tubular toxicity of cephaloridine are related to a carrier-mediated transport system. Possible explanations why significant net cephaloridline secretion does not occur in the mammalians kidney are discussed.
71 citations
TL;DR: The ability of the iris-ciliary body complex to accumulate PGs in vitro and thus, presumably, its ability to remove PGs from the intraocular fluids in vivo, was found to be severely decreased during the course of inflammation, and even several months following an episode of severe uveitis.
66 citations
TL;DR: In this paper, the authors review the considerable progress that has been made towards developing an understanding of the physiological role of mitochondria in the aluminum response and discuss the potential for using this knowledge in next-generation engineering.
65 citations
TL;DR: It is concluded that the apparent carrier mediated PG transport systems of the choroid plexus, anterior uvea and kidney cortex are not related to the iodide transport system, but may represent a subcomponent of the iodipamide transport system of these tissues.
Abstract: 1. Incubation of rabbit choroid plexus, anterior uvea (iris-ciliary body complex) or slices of kidney cortex in a medium containing tritium-labelled prostaglandin F(2alpha) ([3H]PGF(2alpha) or E1 ([3H]PGE1) results in a four- to thirteenfold concentrative accumulation of 3H activity. 2. Addition of PGF(2alpha, PGF(1) or PGA(1), any one of five PG analogues or a PG precursor, arachidonic acid, at a concentration of 10(-4) M reduced the active accumulation of [3H]PGs by 47-97%. Octanoic acid, at the same concentration, had only a moderate effect on the choroid plexus and no significant inhibitory effect on [3H]PFG(2alpha) accumulation by anterior uvea or kidney cortex. 3. Inhibition was also obtained with 2 mM iodoacetate (under anaerobic conditions) and with 10(-4) M diploretin phosphate, probenecid, iodipamide, indomethacin or dinitrophenol. Perchlorate (10(-4) M) and iodide (10(-4) or 10(-3) M) had no inhibitory effect while 10(-4) M p-aminohippuric acid had a significant inhibitory effect on the kidney cortex at a concentration of 10(-4) M and on the anterior uvea at 10(-3) M. 4. It is concluded that the apparent carrier mediated PG transport systems of the choroid plexus, anterior uvea and kidney cortex are not related to the iodide transport system, but may represent a subcomponent of the iodipamide transport system of these tissues. 5. These results suggest that the systemic distribution and the rate of renal excretion of PGs could be altered by high concentrations of PGs, pharmacologically less active PG analogues, some inhibitors of organic acid transport, and by some inhibitors of PG synthesis and PG action.
63 citations
TL;DR: It is evident that aminoglycosides cause multiple metabolic derangements at multiple sites within renal proximal tubular cells, but the available evidence does not identify which, if any, of these drug effects is responsible for initiating the injury cascade.
63 citations